In collaboration with Drs. Shearer and Parker of Washington University of St. Louis, we showed that complement may play a major role in the rate of tumor growth. Components through C3 deposited on a tumor cell membrane, via a mechanism which does not cause sufficient damage to injure the cell (too few complement activation sites), cause a marked increase in the rate of tumor cell growth. Components beyond C3 are not required for this effect. (Reported in the J.E.M.) These complement fragments on cell membranes are of great importance in that they appear to bind to specific receptors which can be demonstrated within tissue sites. In collaboration with investigators in the NCI, a new reclassification of a wide variety of lymphoreticular malignancies has been in progress. More important, within the past year, in collaboration with Drs. I. Green and M. Gelfand, we have demonstrated the presence of a C3b receptor in the human glomerulus. This may explain why complement containing complexes are deposited in this organ leading to the production of renal disease. New and simple methods have also been developed to demonstrate the presence of these receptors, cell suspension in tissue section, which make use of the fact that fluorescein labelled bacteria can have deposited on their surface C3 via activation of the alternate complement pathway. These can be used as a simple reagent to detect C3 receptors.